Hamilton’s rule says that altruistic genes should increase in frequency when rB > C, when r is the identity-by-descent relatedness of the recipient to the actor, B is the fitness benefit to the recipient, and C is the fitness cost to the actor.
r is 0.5 [on average] for your parents, full siblings, and children. r is 0.25 for nieces and nephews.
All of this rests on certain assumptions: random mating, weak selection, linear payoffs, etc. But it’s useful.
Haldane put it into words: “Let us suppose that you carry a rare gene that affects your behavior so that you jump into a flooded river and save a child, but you have one chance
in ten of being drowned, while I do not possess the gene, and stand on the bank and watch the child drown. If the child’s your own child or your brother or sister, there is an even chance that this child will also have this gene, so five genes will be saved in children for one lost in an adult. If you save a grandchild or a nephew, the advantage is only two and a half to one. If you only save a first cousin, the effect is very slight. If you try to save your first cousin once removed the population is more likely to lose this valuable gene than to gain it. … It is clear that genes making for conduct of this kind would only have a
chance of spreading in rather small populations when most of the children were fairly near relatives of the man who risked his life.”
Ron Unz, in one of his occasional visits from Discworld, just offered a criticism of my ‘ gay germ’ theory of homosexuality. He suggests that people would surely develop resistance to any such germ – which general argument must explain why infectious diseases have never been a major problem for humans, right? Why malaria is no problem? The germs evolve too – that’s the point. Parasites can impose fitness burdens for millions of years.
He also says that I ‘viciously insulted’ the intelligence of his old prof E. O. Wilson. Ron does not know what true viciousness is. When E. O. Wilson supported a hypothesis that attempted to explained homosexuality by gay men helping close relatives in ways that produced more nieces and nephews, he sure sounded like an idiot. Because, looking at Hamilton’s rule, they’d have have to produce twice as many of those nieces/nephews to break even – a behavior twice as effective as mother love – which is impossible, of course, in any kind of Malthusian world. Moreover, they don’t even perform these helping behaviors. I am reminded of the time I attended a journal club at the University of New Mexico. They were discussing an article – In Our Genes – that Henry and I had written, so I had unusual insight into what the authors really meant. In the discussion, we (me, Kim Hill, a troop of grad students, and Keith Hunley being twitchy in the corner) were talking about how complex adaptations, in particular behaviors, developed slowly but could be lost rapidly if no longer favored by selection. This robs cave fish of their sight.
In particular, wolves have paternal care, but dogs don’t. Kim and I were discussed how to breed ‘ daddy dogs’ that would have such paternal care, which would inevitably lead to doggy marriage and big money for the Disney corporation, when one young lady in the troop suggest that maybe male dogs did help take care of the puppies, but had managed to keep everyone who ever lived from ever noticing it. Including Albert Payson Terhune and Jim Kjelgaard. Kim Hill, who knows all there is to know about Ache dogs, let alone the Ache themselves, said to her, in a tone of utter finality, “That does not happen.”
That young lady is a deep-dyed bred-in-the-bone idiot – but no more so than E. O. Wilson.
Ron Unz explains that his model took no more than five minutes to produce. I believe him.
West Hunter 
Ron Unz, in one of his occasional visits from Discworld, just offered a criticism of my ‘ gay germ’ theory of homosexuality. He suggests that people would surely develop resistance to any such germ – which general argument must explain why infectious diseases have never been a major problem for humans, right?
That’s some powerfully sloppy thinking. I knew the answer to this the very second I ever heard of the gay germ theory. In fact, I doubt you could even call it thinking at all.
Same goes for the gay uncle hypothesis — but when I was a wee lad in high school, I hadn’t ever heard of kin selection or Hamilton’s rule. Just how do genes even propagate themselves when their hosts do not reproduce? What is one half multiplied by one half?
The best you can say is that there is a major environmental component to homosexuality, and that bearers of “gay genes”, on average, have siblings who are slightly more fertile than the average. (I didn’t know the term for this, either, but I thought it was plausible for a long time.) But that just begs the question of what that environmental influence happens to be. Whatever it is, it sure isn’t hardwired from the beginning. I spent inordinate amounts of time searching for the answer in all the wrong places. What a time consuming way to learn that psychologists are complete morons.
The idea I had at the time was that gay genes have incomplete penetrance (why???), and that on the unusual occasion that they produce a homosexual phenotype, the loss of fitness could be offset by some sort of modest advantage for female siblings. I had heard of a few studies that have found such an effect, but the effect sizes are unimpressive.
I had little proof beyond that, and the idea simply begged more questions than it answered. That’s when I concluded that homosexuality had to be the product of unknown social forces. (If it’s not parenting, and the twin studies say the bulk of the variance is environmental, what else could it be?) What a big mistake, the literature on _that_ is even stupider than psychology.
I probably should have started with a good foundation in biology, but every authority figure I talked to about this made no sense whatsoever, and some of them were downright hostile.
The only way homosexuality could be genetic is if it’s a side-effect of being homozygous for something which gives you a significant benefit for being heterozygous. That doesn’t have to be sexual or altruistic – there’s no reason there couldn’t be some sort of disease-resistance gene which, as a side effect, makes it more likely that a homozygous son born to a mother with a higher-than-normal androgen level turns out homosexual.
If I remember correctly, twin and sibling studies show that there are increased odds of being homosexual if your brother is, but not increased enough for it to be a purely genetic effect. Also, younger brothers seem to be more likely to be homosexual, all else being equal, and there may be some connection to maternal androgen levels, which go up as the mother bears more boys.
So, if the gene requires an environmental trigger to cause homosexuality, its population fitness reduction isn’t very high, and if there’s some unrelated benefit to being heterozygous for that gene, the fitness improvement might be high enough to overcome the fitness reduction from homosexuality. Especially if non-Malthusian conditions are required for the environmental trigger.
I still think the pathogen theory is more plausible, though.
The only way in which you can maintain an allele that is essentially lethal in homozygotes (zeroes fitness) is by a benefit in carriers, heterozygotes. The more common the allele, the larger that heterozygote advantage has to be. The only cases where such dinged homozygotes are ever as common as 1% are all defenses against falciparum malairia, such as sickle-cell or Melanesian ovalocytosis.
Yet you see homosexuality in places where malaria was never a problem. Anyhow, any such allele would stick out like a sore thumb in a GWAS analysis. It doesn’t show up, so it doesn’t exist. No point in talking about it any longer.
Maybe its epigenetic and methylation.
I doubt those claims of increased fertility. So does Michael Bailey.
Never mind, the biology wouldn’t have done me any good, either. Just think of Stephen Jay Gould.
Could ‘biased’ parental investment cause these alleged effects? Send more checks to the heterosexual children?
Hamilton’s rule says that altruistic genes should increase in frequency when rB > C
How does that work in the case of males who lay down their lives for the group?
While I can see that the sum of riBi could be greater than C for that person’s immediate relatives, but those relatives (offspring especially) would have to survive to reproductive age, and the loss of the support of their father might be a problem.
“How does that work in the case of males who lay down their lives for the group?”
Probably helps if you marry them as young as possible so they mostly already started reproducing before they get killed.
“and the loss of the support of their father might be a problem”
Lot of Germanic tribal laws specified brothers marrying the widows of their brothers.
My guess is as soon as this stuff extends beyond very small, very closely related bands it starts to need cultural reinforcement to make it work e.g. you make the cultural reproductive penalty for being a coward worse than the penalty for being brave.
“Lot of Germanic tribal laws specified brothers marrying the widows of their brothers.”
By the way, that practice is also common in many West African tribes.
Deuteronomy 25:5, too. Sort of.
If you write the Hamilton formalism as a differential equation and look carefully it is apparent that the selection has to affect fertility but not mortality. The reason is that my own inclusive fitness includes what I do to others. If I die then I can’t have an effect on others but if I am infertile I can still have my effects on others.
“How does that work in the case of males who lay down their lives for the group?”
If failure to do so results in the extinction of the group (including you) then there would be strong selection pressure.
“How does that work in the case of males who lay down their lives for the group?”
Battle of Thermopylae circa 480 BC, the only Spartans who went with Leonidas were ones who had already produced sons. So they had “banked” the Spartan gene pack (warrior, patriotic, etc). Compare this to the men of Europe who fought in WW1, and many of them I’d bet were single, and particularly the French and English saw a culling of Patriots (and the related genes) This was so bad that the next generation had difficulty deciding it was worth facing a renewed German threat.
Horseshit. Do the numbers.
Here: http://www.dailymotion.com/video/xz2jjx_cross-cultural-differences-in-newborn-behavior_news
Hello,
I, Not Ron Unz, would like to reply by ignoring/misunderstanding everything that you’ve just written.
Further, I’d like to draw your attention to “cherry-picked quote,” from the textbook of Authority Figure #1. What sort of cruel man would disagree with Authority Figure #1?
And what about these statistics from weak sources? Do you disagree with the gospel of Authority Figure #2’s data-gathering ability?
In sincerest pomposity,
N. R. U.
Hahahaha !
You’re clearly right here, but I’m impressed at your willingness to bite the hand that feeds you. Really, it’s kind of confusing for a casual observer why Unz gave you a big pile of money. On the internet it seems like the main form of interaction involves you tearing apart his half-baked theories, while he protests. What’s in it for him?
It is less of a mystery than you think, because he stopped giving me money – which is his perfect right, of course. When I was on the teat, he would send me an idea and asked me what I thought of it. I was polite, but mostly I thought he was wrong, and told him so. It may be that he didn’t like that. I don’t think there have been big short-term gains in Irish IQ, I don’t think that Mexican immigrants continue to converge academically (after the initial improvement from acquiring English), and I don’t think Rambo was right. I don’t think that Vioxx killed half a million people – more like 30-45k. I don’t think that the Soviets were within two weeks of launching an offensive against Germany when Hitler attacked in 1941. I think the BJS statistics on Hispanic crime rates are more reliable than Ron’s thoughts. Let me tell you, I kept hearing him say ” well, that fact that apparently contradicts my thesis could well be explained by something I just thought up” – and then he’d act as if his speculation was a proven fact. Since academic achievement among Hispanics in New Mexico is still low, even thought at least half of them have been here for hundreds of years – Ron just knew that there was some special mechanism in New Mexico that indumnified them. Actually I’m pretty open to that idea in general, because there is certainly something wrong with the state – Walter Jon Williams thinks it’s a fungus – but none of the events he suggested as causes seem to have actually happened.
As for the Harvard thing, pro-Jewish discrimination in admissions, Ron uses one method to estimate Jewish National Merit Finalist numbers [last name analysis] and another very different method to estimate the actual numbers admitted – quoting Hillel as an authority. It seems that you get a far lower number. if you apply that last-name analysis to Harvard too. And the National Merit threshold varies by state – it is higher in the states where most Jews live, which would depress their numbers of finalists, all else equal.
Moreover, it surely matters who even bothers to apply to Harvard – but nobody knows that, outside of Harvard. I had pretty high test scores, and got letters from quite a few colleges, including Harvard, but I never applied there, because (among other considerations) I didn’t think much of the place. I still don’t. He also ignores geographical proximity – most Jews live in the Northeast. As I remember, proximity was one of those other considerations for me, since I needed to be able to take my laundry home on on the weekends.
If there’s something wrong with New Mexico, at least it seems not to affect Los Alamos.
They’re not what they used to be – haven’t developed a new superweapon in years. I have a good friend up there in X division. Years ago, I said that if they ever ran into something stupendously important and needed people, I’d be happy to join. They wouldn’t have had to tell me anything about the discovery – his word on its importance would suffice.
That word never came.
I think you’re wrong.
Disney just has to do a film on the free-ranging dogs of India:
http://www.journals.elsevierhealth.com/periodicals/applan/article/S0168-1591(04)00175-3/abstract
“Six lactating bitches”
female dogs!!
and have to say, during some boring days observed the same phenomenon. Daddy dogs keeping the brood in line. beta asian dogs?
Did they observe all male dogs?
This just says that there is variation and not all domesticated but wild dogs have lost the genes for male involvement in the offspring.
Cherry picking?
The difference apparently being that those Subcon Indian dogs are completely feral and have no regular, ongoing connection with any human group. So, like Dingos, they have a tendency to revert to wolf-like social behavior.
What did you think of Unz recent big paper on Asian/Gentile discrimination and Gelman’s critique of it?
“had managed to keep everyone who ever lived from ever noticing it”
So much of leftist social “science” seems to rely on this kind of implausible action-at-a-distance/conspiracy-theory sort of thing. I mean, “White Privilege”–is that something you’ve seen? In the academic job market? At tenure reviews?
Of *course*, I’m aware of all those Hamilton inclusive-fitness issues, and quite possibly have been for much longer than gcochran, given my strong interest in the topic stretches back to the late 1970s. And I also agree that E.O. Wilson is almost certainly mistaken on the Gay Uncle Hypothesis, but since the Gay Germ Hypothesis seems just as ridiculous, I don’t think the harsh insults to Wilson’s intelligence were warranted.
Consider the Gay Germ model. I don’t think that anyone has ever suggested that the germ actually transmits itself via the sexual behavior in question, so that behavior is seemingly a inessential byproduct to the germ life-cycle. If the behavior doesn’t matter to the germ, but obviously matters very, very much to the genes of the host, there would be powerful selective pressure upon the germ to drop that particular extended phenotypic expression, after which the host would declare a permanent truce in the evolutionary arms race. After all, the human body is filled with a multitude of free-riding germs, so who cares about a few more?
GCochran correctly points out the *massive* selective pressure against gay behavior. So if the germ didn’t really need it for anything, why keep it?
This is *extremely* different from the case of nearly all infectious diseases, in which the harm inflicted upon the host is directly related to the massive multiplication or propagation of the germ. If gays ran around biting straights and thereby turning them gay, then I’d agree that a germ was probably responsible.
Ron, paralyzing people never helped spread the polio virus, which is essentially an intestinal bug. But it happens. I have no reason to think that making your fingers fall off helps spread leprosy – yet it does make your fingers fall off, eventually.
Tertiary syphilis gives you interesting delusions of grandeur – but it’s not very infectious at that stage. The delusions don’t seem to help spread the bug. It just happens.
A better example: suppose that some enterovirus gained by molecular mimicry. it is shielded to some extent from the immune system, because it looks very much like some host protein. Now this occasionally triggers an autoimmune reaction – which doesn’t really benefit the pathogen, although the mimicry itself does. That’s what happens in type-I diabetes. There’s a similar story with rheumatic fever.
Men who have sex with men have much higher rates of STD transmission, which could be helpful in spreading some organisms. But a pathogenic cause couldn’t be solely STD (something has to infect the kids with it, although HIV can be passed mother-to-child.
If one were looking at an STD there would be big visible systematic differences in the parents of gay men, so this probably could and would be falsified quickly. What transmission mechanisms are you thinking of?
Look, none of this is very complicated. Why do hosts oppose the presence of infectious disease germs (or any other type of parasite)?
(1) The germ may convert substantial portions of the host’s nutrients or biomass into more germs.
(2) The germ may clog up or otherwise disrupt the host’s functional systems in order to propagate itself throughout the host.
(3) The germ may alter the host’s behavior in ways that are harmful to the host but necessary to transmit the germ to other hosts.
Now let’s consider which of these symptoms are found in individuals infected with the alleged “Gay Germ”:
(1) Nope.
(2) Nope.
(3) Apparently not.
So as near as we can tell, the only negative impact of the alleged germ is to alter the host’s sexual behavior in a way apparently not beneficial to the germ but *massively* harmful to the host’s genes. This makes absolutely no evolutionary sense for an infectious disease.
One of the problems with your particular disease examples is the same one you use to attack Wilson: the huge selective pressure involved. I really don’t think 3% of every generation got paralyzed by polio before reproducing, and I similarly doubt that leprosy or syphilis generally had a 3% impact on the reproductive fitness of a population. And in the case of the hypothetical mimicry, the harm inflicted is directly, causally related to the needs of the germ to safeguard itself.
A 3% hit to reproductive fitness is HUGE—the host population will evolve rapidly to protect against something like that. And if it’s a useless byproduct of the germ’s activity, the germ will be under strong pressure to modify it and declare a truce with the host.
For example, I just checked on Wikipedia. In the 1916 American polio “epidemic”, there were 27,000 total cases, most of them probably not crippling. The total population was over 100M. That’s a rate of 1/4000, absolutely trivial. And remember, that was an “epidemic” year.
Offhand, I’d think that the vast, vast majority of harmful infectious diseases produce harms that are directly linked to the necessary activities of the disease. I’ve never heard of a *massively* harmful disease in which the harm isn’t necessary to the disease. Sounds needlessly malicious to me.
Until you can propose *some* plausible reason why a Gay Germ needs the gay part, you’re far behind where Wilson was. At least he came up with an explanation, even though it was wrong and silly. But you haven’t yet proposed any explanation at all.
Chlamydia often causes sterility. There are parts of the world – Africa’s ‘sterility belt’, where tens of percent of women were sterile or had drastically lowered fertility, before antibiotics became widely available.
According to your argument, that can’t have happened. But it did.
Enough already. Your style of argumentation is not productive.
Aren’t sterile women in those African societies usually forced into prostitution? Hasn’t there been quite a bit of speculation in ev-bio circles that the sterility inflicted by the disease therefore greatly increases the effectiveness of its vector transmission to additional hosts? Now *that* is an ev-bio disease hypothesis that makes perfectly good sense to me.
By the way, the host could simply respond by evolving a different version of the endogenous molecule that makes it hard to differentiate parasites from healthy tissue.
One that is sufficiently different from the pathogen to allow efficient recognition of self from non-self.
Except the pathogen could do that, too. And that’s exactly what that does. New HIV medications typically last about six weeks before a resistant strain evolves somewhere in the world.
It could be that the germ causes a small increase in fertility in most hosts and homosexuality only in a fraction of cases.
In response to Ron Unz on African veneral sterility:
I have spent a lot of time in the southern half of the infertility belt, also called the ‘sterile crescent.’ There was no market for prostitution there–too much amateur competition, but the women were certainly, er, active. I think the idea that infertility pathogens would be selected to increase activity is a good one. Hard to sort out cause and effect here of course.
A common strategy for pathogens to colonize new tissues of the body, or to even evade the host’s immunological defenses entirely, is to cleverly mimic the biochemical machinery that enables communication between different cells of the host.
For instance, T cells are not rational actors — in most individuals, they cannot tell the difference between the body’s endogenous ligands for the chemokine receptor CCR5 and the surface proteins of HIV virus. The former serve a useful function in the body, while the latter leads to a noxious disease that slowly decimates the immune system, culminating in a humiliating death and an impromptu visit by the Fred Phelps clan. Now, does the latter ever facilitate the reproduction of the pathogen? No. When it comes to infectious diseases, is this sort of phenomenon especially uncommon? HELL NO.
A lot of autoimmune disorders are known to occur the same way. For a while, the pathogen thrives undetected in the host by mimicking some useful macromolecule that is needed elsewhere in the body. Could be a cell surface molecule of the MHC. Could be the receptor for a certain neurotransmitter. It could even be a small cluster of cells in the pancreas, ones that produce insulin. The point is that this strategy works because the immune system would otherwise go haywire and destroy normal parts of the body. And that could seriously impair your reproductive fitness.
Except, oops, sometimes that really does happen. You see, there is an evolutionary trade off between an immune system that is especially neglectful, and thereby avoids harmful (and unnecessary) responses to innocuous substances in the body, and one that reacts to potential pathogens in an especially vigilant manner, thereby minimizing the risk of infectious disease. (Just ask anybody who suffers from hay fever what that’s all about.)
What would you expect might occur if a certain immune system recognized a certain pathogen by a foreign polypeptide that was similar in sequence to a native protein that is endogenous to the host tissue? What if the two were so similar, that it couldn’t tell the difference between the two, and attacked both willy-nilly? Are there any known examples of this in the literature?
Now, what if that tissue happened to be someplace in the hypothalamus? What if it happened to be a cluster of neurons that regulates the sex drive during puberty?
And why might anyone think it would be an especially poor evolutionary strategy for the immune system to evolve to be ever more vigilant in the destruction of that pathogen?
speaking of vigilance, there is evidence that risk alleles for Type-I diabetes in Europeans have experienced positive selection. Looks as if they made you less likely to die from certain kinds of diarrhea, but increased susceptibility to Type- I diabetes.
Native Americans are the least likely to develop autoimmune disorders, if I recall correctly?
So homosexuality is an auto immune response?
The gay germ theory makes a great deal of sense. Any ideas as to when/where/how transmission might occur?
Mostly before adulthood, surely. More likely a virus than a bacterium, mainly because we’re drenched in antibacterial antibiotics nowadays, although anything is possible with gut bacteria.
I had a sentimental fondness for a parasitic worm as the cause, but you don’t always get what you want.
You convinced me that it can’t be heritable. But why germs as opposed to other nonheritable, environmental or developmental causes?
“The gay germ theory makes a great deal of sense” Gays should be segregated to prevent disease spreading. lol.
It is probably not the pathogen that attacks the cluster of neurons directly. That would be stupid, and pointless, because there aren’t very many in the body as it is.
It is probably the immune system, in a minority of individuals, reacting to a common pathogen along with any other cells of the body that express similar surface molecules. These are pattern-specific, and are often limited to precise locations of the body.
Interresting, I find it quite convincing as a mechanism.
Now it means that it is better for the immune system to target the pathogen, even with this not so small risk of overeacting. The pathogen can not be that benign to begin with, else the immune system would be tuned down, to reduce the chance of overeaction, at the price of a small chance of letting the pathogen run wild.
Should be some balance in there, intuitively, we may find the pathogen occasionally killing and severelly maiming people whose immune system is at the other spectrum, ie much less likely to have auto-immune reaction in the hypothalamus, but slightly less effective controlling the bug.
Do we see that? Is there a bug that is common in newborn or toddlers, that is usually kept at bay, but sometimes is severe or fatal? Maybe some kind of equilibrium with the gay-inducing overeaction would allow to compute the prevalence of the illness (times his reproduction reducing effect) (1% if it kills regardless of sex, which would be the same as the 2% gayness in males (assuming it reduce fitness to 0 ).
Do I make sense, or is it complete rubish?
Koch’s postulates are really hard for these sorts of pathogens. For one, why would we expect the virus to stick around after the immune system has reacted to it, thereby causing the autoimmune disorder?
For something like narcolepsy, theory SCREAMS that a pathogen is responsible for the vast majority of cases, yet none has yet been identified. For one, nearly all patients have the same HLA allele. Two, nearly all narcoleptics are missing a small cluster of neurons in the hypothalamus that generate hypocretin, a hormone that is responsible for the regulation of sleep. Otherwise the are totally normal. The cells were there before, and now they’re gone – what happened? The immune system is readily capable of something like that, and we know how it happens. Lastly, it has a low heritability, and yet it exists at a frequency that is much higher than any genetic disorder that has no heterozygote advantage. (Genetic narcolepsy, where sufferers are born unable to synthesize hypocretin, does exist, but it is correspondingly rare.) Only a pathogen would fit this pattern.
For all sorts of other viral diseases, identifying the virus is usually not hard, because it *directly* is responsible for the disease and is abundant in the tissue. To find the gay bug, we would have to find it before it even hits, which is a total waste of time.
And yes I do propose a balancing act between an active and underactive immune system. Molecules are dumb, and any immune system would have a very difficult time distinguishing between a molecule which is expressed only in a tiny cluster of cells (GOOD), and a molecular mimic by a virus (BAD). An immune system that tried to destroy the latter might easily end up destroying the former. The pathogen could just keep evolving to make its molecules more and more like those of the host, making things even more complicated for the immune system.
I think it is time to go back to basics. Simon LeVay published a study suggesting that gay men have an unusually small variant of some nucleus in the hypothalamus, but the sample size is unimpressive, and the gay men were all AIDS victims. We will have to start looking for increasingly fine differences in anatomy between gay and straight male brains. Hard thing to do, because whatever that difference is, it has to be in a very small region of the brain. If we found the offending cells, we could see what sorts of surface proteins or other epitopes that are unique to that region only.
If we were sure about the exact anatomical difference in rams, the only other mammal in which lifelong homosexuality is known to occur, we could do a comprehensive immunoassay with common pathogens found in lambs. It would be much easier to find funding for this, and not for that other species, and the livestock industry might fund it. (Or maybe not, because artificial insemination exists, they might not care whatsoever.)
By the way, are there any HLA alleles that are especially common among gay men? Has anybody bothered to look? I don’t see anything like that in the literature.
The data exists, and I knew someone who wanted to take a look at it, but they wouldn’t release it.
Jerks.
Someone might could try again.
On second thought, if HLA mattered, it should have shown up in that GWAS study. Didn’t.
Never mind about that. I wouldn’t expect to see that for a condition that affects 2-4% of the male population. Unless there were some fitness trade-off somewhere.
Your math (“they’d have have to produce twice as many of those nieces/nephews to break even”) appears to suppose that gay men never reproduce, which is false.
In recent history, most gay men married women and had children. It’s only acceptability (and contraception) that has partly changed that, and it’s still fairly common.
Presumably, there’s some reproductive hit. Do we have any numerical information at all on how much less gay men reproduced in the EEA than straight ones?
Depending on the value of that parameter, incomplete penetrance or even E. O. Wilson’s theory might work.
Your math (“they’d have have to produce twice as many of those nieces/nephews to break even”) appears to suppose that gay men never reproduce, which is false.
The “math” proves that gay men would have to work harder for the sake of their nieces and nephews than worker drones do for their siblings. No such pattern exists in any culture on Earth, either past or present. Homosexuality is not ubiquitous across human cultures. The Mbuti pygmies still have no clue what it is, and it’s not like they’ve been hiding their gay men from the prying eyes of anthropologists out of shame. They tolerated Colin Turnbull just fine, and he was a prancing sodomite who was thrilled to demonstrate his “expertise” on more than a few of the young boys. (Some men like dark chocolate, others prefer vanilla cake.)
As for gay men getting married and having kids, do you realize that they would have to compete men who *actually* dig women, and that historically speaking, far fewer men than women managed to reproduce? (By the way, how do we know _that_?) Even a fitness loss of 5% would have eliminated any gay alleles from the gene pool long ago. They would have to be continually replenished by random mutations.
Either way any debate over the existence of “gay genes” is moot — the twin studies show low heritability, the GWAS studies have come up with exactly zero, so they probably don’t exist. That was easy.
While helping a friend who is a psychology major with his homework, I noticed that his developmental psychology textbook cites Dean Hamer’s research as proof that homosexuality has a strong hereditary basis. Yeah uh-huh. You keep being stupid.
How do you figure that most homosexual men got married and had children? You’ve got no numbers for that, I’m certain.
Not getting married is easy and always has been, unless you’re the heir to a throne. Plenty of heterosexual men have done so for ages. And not being married excuses you from breeding. Those few homosexuals who had offspring would be a small fraction of a small fraction, a biological dead end.
And how much more likely would a homosexual man’s wife be to have an affair and possibly cuckold her husband, so falsifying the records which said that particular gay man had children?
One interesting implication of this is that malaria shows a pretty huge selective effect in the genome.
Malaria adaptations are one of the most obviously honking great signposted positive selection signals in the human genome.
So that should be the case for a homosexuality pathogen as well. The fitness effect would be of a similar scale.
I think it’s pretty obvious that the whole elegance of a germ explanation is that the environmental factor would coevolve to keep step with selection. That’s what makes it more preferred than a model with some other environmental factor.
Vulnerability to non-germ environmental hazards can stick around for a very long time as well, but then it is immediately obvious why the case (it’s obvious why we haven’t evolved a biological response making us immune to drowing, even though it pretty bad, because the cost relative to the fitness benefit would be too high to ever be practical on a human biological framework).
Still, I think it’s useful to try and recognize that if there is a pathogen, it is working against huge selective pressures for immunity, its trying to hit a relatively small target (Dr Cochran has described this previously when talking about mutational load explanations), behind the blood brain barrier and has avoided detection so far (although us not looking would help a little with that).
This kind of pathogen and adaption should also be ubiquitous across nature (for instance, across great apes). It’s not like malaria just likes humans.
Still, I think it’s useful to try and recognize that if there is a pathogen, it is working against huge selective pressures for immunity, its trying to hit a relatively small target (Dr Cochran has described this previously when talking about mutational load explanations), behind the blood brain barrier and has avoided detection so far (although us not looking would help a little with that).
You, along with quite a few other people, seem to believe that the pathogen works by directly attacking the brain itself. I think we may conclude a priori that such is not the case. For one, gay men aren’t mentally retarded, they aren’t epileptic, and they don’t see hobgoblins lurking behind every bush. They are at a higher risk for certain things like depression and bipolar disorder, but you don’t need to appeal to neurobiology to explain why they are promiscuous, or why they have a shorter life span than the average.
Whatever the hell is responsible for homosexuality, it has to be the destruction of a small cluster of neurons that is responsible for a specific function. (We see similar patterns in the brains of gay rams.) Any pathogen that worked by directly attacking those cells would soon be a goner. First of all, there aren’t that many cells to go around, so it would have limited opportunities to propagate itself. If that were the case, evolution would probably favor the immune system of the host. Secondly, even if it did directly attack the brain, we might as well assume that it causes some sort of behavior that makes it really easy to infect new hosts. Anything else would be suicide for the pathogen. Just what might that be? Child molestation? The inhalation of hairspray? Lip-synching to Judy Garland films?
The pathogen should thrive best in a situation where a stronger immune response would be inimical to the fitness of the host, while a weaker immune response would allow it to spread with impunity, which might again impair the fitness of the host.
Misdreavus,
Roselli, the sheep researcher, seems intent on concentrating on hormonization irregularities in utero. You seem really up on his work, which for a long while seemed to focus on a hypothesis that aromatase, which catalyzes testosterone into estradiol, was responsible for a difference in brain structure between male-oriented rams vs female-oriented rams. He has established that masculinization of the genitals takes place in utero earlier in gestation than
masculinization of the brain.
I haven’t followed his work in a while, however. Last I read he was looking for an androgen receptor mechanism, and I don’t know what he may or may not have discovered with either that or aromatase.
In any case, do you know if he has done any experiments that focus on fetal exposure to a pathogen or the pregnant ewe exposure to such? In that same vein, wonder if he’s aware of Dr. Cochran’s hypothesis-it might offer a quicker avenue to understanding hormonization atypicalities, if indeed that is what is occurring in the affected rams.
I don’t buy it. In fact I think the whole hormone hypothesis is stupid. The idea that differential exposure to androgens in utero might cause very specific, localized patterns of damage to the hypothalamus doesn’t make a lot of sense. You can guarantee that this won’t be the case, because androgen receptors exist in a lot of places other than the oSDN nucleus (which is apparently larger in straight rams than it is in ewes), yet this is the only reliable difference in brain anatomy that Roselli has found between gay and hetero rams. Has anybody ever heard of a case where exposure to testosterone induces hyperplasia in the psoas minor muscle (and nowhere else)? We don’t see similar patterns in human beings, either. To the best of my knowledge, I’m not aware that monochorionic twins are any more concordant in homosexuality than dichorionic twins.
But an autoimmune response might do exactly that. The immune system is very good at discriminating between increasingly fine molecular differences between tissues in the body, or even specific parts of a tissue from another — in fact that’s just what it evolved to do. Androgens generally don’t. Go visit your local gym and see just how many roid monkeys have backs covered in acne.
And of course, exposing ewes in the womb to testosterone should increase the size of the oSDN nucleus, if that does happen to be a sexually dimorphic trait. But this most likely results from masculinization of the brain as a _whole_, not site-specific changes in mRNA transcription.
I think Roselli is most likely confusing proximate and distal causes.
(Comment above was mine)
Thanks for your input re Roselli’s work.
Thanks for the response. Cochran’s response below on an estimation of the fitness cost is interesting as well.
If I’m understanding this right, the idea is that the pathogen plays “chicken” with autoimmune system – too high and a brain region which has similarities to the pathogen gets it from autoimmune system, causing homosexuality and thus sterility, too low and the organism is burdened with the pathogen. So assuming this is correct, would be looking for a pathogenic condition which gay men do not get (because their body’s over zealous autoimmune system has wiped it out, along with part of their brain)? It seems like kind of the inverse of the idea that gay men are carriers of the pathogen, since under this scenario, that is the one thing they are not.
And of course, exposing ewes in the womb to testosterone should increase the size of the oSDN nucleus, if that does happen to be a sexually dimorphic trait. But this most likely results from masculinization of the brain as a _whole_, not site-specific changes in mRNA transcription.
Sex dimorphism is supposed to be tough to evolve. While this wouldn’t be enough to explain homosexuality, for the reasons Cochran has explained ad infinitum, perhaps might explain variation in the size and redundancy of the relevant brain region(s) (presumably which inhibit same sex attraction signals, quashing the kind of signals which would go nowhere in the heterosexual brain) in normal males or females. Thus explaining robusticity in the face of an autoimmune response and thus prevalence of homosexuality. That would explain the femininity / masculinity correlations with homosexuality.
That’s a tricky conundrum. Molecules are stupid. DNA polymerase, after billions of years of evolution, still can’t distinguish between harmful proviruses and host DNA.
The selective impact is probably ~10-20 times smaller than that of falciparum malaria.
Matt
“Still, I think it’s useful to try and recognize that if there is a pathogen, it is working against huge selective pressures for immunity”
Maybe it’s adaptive in one environment but not in others so the effect is proportional to contact with that environment. People keep mentioning the 4% figure but was it always 4% and if not how recently did it start to go up?
“This kind of pathogen and adaption should also be ubiquitous across nature (for instance, across great apes).”
Maybe it is but they and the Mbuti have developed an immunity?
Diseases often have different symptoms in populations that haven’t been exposed to the disease/co-evolved with the disease. Could homosexuality (the permanent, non-reproductive kind) be a relatively new phenomenon in Eurasia, maybe something that broke out during the Age of Exploration or of imperialism? Populations with no homosexuality would be candidate areas for where the hypothesized diseases came from.
Doesn’t seem likely, but for what it’s worth.
J. Cotton
“By the way, that practice is also common in many West African tribes.”
Makes perfect sense.
Marrying your brother’s widow is commanded by the Torah as well. Onan, as in “onanism”, was condemned for masturbating instead of screwing his dead brother’s wife.
What Onan did was pull out, i.e. withdraw prematurely, i.e. practice coitus interruptus. Genesis 38:9.
L’Esprit: My Genesis says “…spilt his seed on the ground”. Six of one, half dozen of another.
This was “when he went in unto his brother’s wife”.
L’Esprit: I thought that “…Went in unto…” referred to going inside his sister-in-law’s tent. But I guess you’re right.
I find it humorous to be talking about a pathological response to something that seems well embedded in the human experience range with thousands of years of history across the planet. If we haven’t yet arrived at sufficient stability to eliminate most of these http://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?mode=&term=Chromosome+disorders from our reproductive outcomes, what makes us so sure that a small deviant abnormality that has been repressed for much of civilization through cultural norms would be eliminated. My experience with people in the gay community shows that quite a few of them from more conforming religious backgrounds had children, in some cases numerous children, while still pursuing a hidden lifestyle. Only after the repression ended, did their marriages end, and open expression of their chosen lifestyle emerge. Even in looking at other cultures, significant interactions occur between males, with a dominant partner not considered homosexual. So, while I think there is a slight potential for the immune system reaction hypothesis, I also think there is also a genetic predisposition inherent in some part- and that predisposition should be apparent to anyone who is spending time talking about finer variations in intelligence based on genetic differences based on origin and genetic clade.
As I stated above, that a minor factor in reproductive success should not be selected out, given a quick look at the imperfect transmission of genes in the human genome, is not a surprise.
It is exactly as surprising as 2% of the human race frantically poking sharp sticks into their eyes. You’re just used to it.
All theories about gays might end up with nothing. I wonder people will theorize why some people had car accident. Traffic accident genes or germs?
At end, gays are just natural accidents like traffic accidents.
Nearly everything reminds me of something, even dipshit comments like this. Once upon a time, an analyst at State Farm Insurance (Sam Boyden) noticed an odd and dangerous pattern of severe tire failure from tread separation. He was a car guy, and he knew that just wasn’t right. On further investigation, it turned out that the bad tires came from the Bridgestone (formerly Firestone) plant at Decatur, Illinois, that had recently gone through a ball-busting strike. It wasn’t caused by incompetent strikebreakers, but by pissed-off union workers. Sabotage. Those tire failures killed about 70 people.
It would have been difficult to make a case, but there should have been an effort to find and prosecute the workers responsible. Firestone workers had a real grievance, since the new owners were pushing for one of the most abusive contracts in history, but they should have settled it like men, by beating the living shit out of key corporate decision-makers.
Parenthetically, this country would far better off if the jackasses and thieves who run the country were far more afraid of the average guy. Pinkerization has a downside.
“they should have settled it like men, by beating the living shit out of key corporate decision-makers.”
It’s comments like this that keep me coming back to this site. Cochran for President! (Or at least Secretary of Labor…)
Glad someone agrees with me!
Professor, what you’re advocating is called “domestic terrorism”… You of all people should know better than to share our plans in plain view of the Galactic Empire.
Obviously my dipshit comment is thought provoking enough to get a reply.
“When American piss is the elixir of life – that is national greatness.”
My shit is a personal greatness. Kidding.
Joke aside, Jewish temperament is well demontrated here as well as documented by British (who often have opposite temperament) in following article.
http://www.bbc.co.uk/news/magazine-22089936
You have a point…
Like traffic accidents where a guy gets rear ended.
Ahahaha!
Question – what kind of evidence, and how it could be obtained, that would disprove ‘gay germ’ theory? I am trying to understand how falsifiable this theory is.
Finding a genetic cause.
Finding a non-pathogenic environmental cause.
Homosexuality would be a benefit to maintaining armies. Alexander the Great’s Asian campaign lasted 11 years. A soldier who is in the army for life can have the years of training necessary to operate a phalanx or legion. Such an army can win against hordes of Persians or Britons. A life spent in a fort and on campaign would be less disruptive if you were gay. A civilization with more homosexuals could have an easier time getting men to be career soldiers.
So these gay soldiers are going to do what – rape the women in the lands they conquer? How’s that gay gene of theirs supposed too spread. Sure, buggery happens when there’s no women around, but that’s a far cry from not being attracted to women when they’re available.
If you prevent the enemy from razing your city and sewing the fields with salt, you would give a survival benefit to male relatives.
A ton of wasted altruism, if you ask me. You can’t possibly make the math work out in your favor.
We do know that celibate military orders have been highly effective soldiers. Fletcher Pratt wonders why there are no good theories on why that should be.
http://www.psychiatrictimes.com/schizophrenia/content/article/10168/2137284?pageNumber=1
Having read to the bottom of the list of comments, I decided to turn to other matters, and immediately bumped into this little study, tentatively suggesting that infections are a frequent cause of relapse in schizophrenia. Given the above comments, I show it simply to illustrate how much standard psychiatry/psychology ignores infection as a cause of behavioural change.
That’s interesting. I’ve noticed that I get wrist-slittingly depressed 2-3 days before I get a cold. It’s not feeling bad from being sick: doesn’t happen with flues or whatnot that are physically worse. It’s not psychosomatic either, because it’s the first symptom.
Over at TAC, Ron Unz is suggesting that Greg has banned him from commenting at this site.
I hope that’s not the case.
First, whatever one thinks of the quality of Ron’s argument, he was making an actual argument. He wasn’t being disruptive or loony. Yes, he might be given to overly elaborate and uninformed arguments in which the word-to-sense ratio is lower than average, but his points could have still been usefully countered rather than censored.
Second, HBDers are routinely harassed, blackballed, and suppressed – often with little justification. I believe many of Cochran’s arguments on various topics, from the war against Iraq to HBD, have been removed from several high profile blogs and forums. So while I understand Cochran’s desire to cull some of the idiotic and disruptive posters who occasionally wander in to share their opinions, I would hope his own experience would cause him to go easy with the editorial guillotine when a poster like Unz is making an argument.
Third, a lot of people like a good dustup, and last night was a good dustup. I was reading the back and forth in real time, and it was highly enjoyable. Cochran is very good in these verbal battles, and they’re often highly edifying for those on the sidelines who get to view them. Too many intellectual discussions are stuffy because the participants are either overly collegial or afraid to give offense. We rarely have that problem at this site That’s one of its beauties.
I hope this is just a misunderstanding. But if Greg has banned Ron from commenting, I also hope he reconsiders his decision and invites him back to finish the discussion. I for one would look forward to reading it.
Of course I banned him, and good riddance. He’s a waste of time. As a friend with a fair amount of experience said, Ron is impervious to reason.
I mean, he comes with up wrong ideas about everything, and then he goes on and on forever, arguing like a possessed lawyer. Who needs that?
Greg,
“Who needs that?”
If you were tasked with actually changing Ron’s mind or matching his arguments word for word, then I wouldn’t blame you for banning him, for you won’t be able to do either one of those two things.
But of course you need do neither. You can instead focus on the few valid points he makes or play off his comments like you do with the occasional uninformed post which entertains you (“Nearly everything reminds me of something, even dipshit comments like this….”).
By cutting off the debate, your readers lose. We’re deprived of both your informed arguments and some entertainment value. It’s not a matter of you getting in the last word, but of countering what valid arguments Ron has by showing how uninformed they are. Just ignore the rest.
I am ignorant of most of the science discussed here, and I find it hard to follow Ron Unz’s comments, as well as a lot of other things I read, but I think it’s useful to allow the benighted to have their say. There are always non-commenting readers willing to be educated, and refuting error is good teaching.
As someone trying to learn from you – I need that. Seeing “wrong” allows skeptical mind to lock onto “right”.
Please unban him. This is one of preciously few places of intelligent debate. Even the discussion above re: pathogens should never cause needless damage –> but yet they seem to nonetheless was really interesting from a spectator point of view. Take one for the team.
Who needs Ron Unz with his theories? Actually I’d say all of us, in that he at least presents theories with evidence. His reasoning may by incorrect but you still have to go through it to figures what he has said. I find a great many people waste my time. I wish I had an oracular source that was 80% correct. It would save me a lot of time — but I have not found one.
After ten vigorously wrong notions in a row, I gave up. I think your filtering method is suboptimal, Jerry.
I noticed this morning that a post of Ron’s and two posts of Misdreavus were stuck in the spam filter. I released them.
Think of the opportunity cost. When I’m responding to Ron, I’m not responding to you – and you’re more interesting. Also, although you may enjoy seeing me endlessly refuting his crap, I don’t. I’ve already had my fill of that. Once upon a time, I used to belong to a closed list, with a fair number of supposedly high-powered people. Some knew their field, but most (opinion writers for example) apparently didn’t know jack about anything. Of those that did know their field, most were clueless yet confident about everything else on Earth. I spent too damn much time explaining that the Russians did most of the fighting in WWII, that Alexander did not die in battle, that educational achievement in America has not cratered, that bombing would be effective against the Taleban in Afghanistan in late 2001 [JDAMS]. There were better moments. I fondly remember talking a lot with Jim Chapin: he was a democratic socialist, not my exact cup of tea, but when we talked history, it was the same history. Many of the other members felt that they were entitled to their own facts.
But on the whole, it drove me crazy. Someone – damn near everyone – was wrong on the Internet, and apparently I was the only who could resist them. No more of that.
Greg, where did you end up going to college instead of Harvard? Wikipedia mentions the University of Illinois, was that for grad school or undergraduate, or both? Just curious.
University of Illinois, undergrad and grad. I got to like the place. Excellent pizza, for one thing: anyone here familiar with Papa Dels?
Perhaps the banning of Run Unz is intended to serve as an indicator of reduced fitness? Those of us who survive this blog will go on to procreate: procreate ideas and followers at the very least, though probably not children, not among each other anyway.
In that case, Justin Bieber has orders of magnitude more “fitness”. Any ideas JB might have will out-reproduce anything conceived on this blog.
Show you off. Tonight I wanna show you off.
Greg,
Did you know Roger Ebert while you were at U of I?
I learn a lot from you, even when I disagree with your opinions. Keep up the good work.
Didn’t, he was well before my time.
Bring back Ron Unz!
@LesserBull
“Diseases often have different symptoms in populations that haven’t been exposed to the disease/co-evolved with the disease…”
Yes, i don’t have a view on how likely it is just that it might square the logical circle vis a vis high immunity and low immunity responses.
Pingback: Linkage | Uncouth Reflections
If you don’t come home some night, my guess will be you stopped for a drink and had a bar fight.
Pingback: Gay Germ Censorship | The American Conservative
Pingback: Gay Germ Censorship | Ron Unz – Writings and Perspectives
Pingback: Gay Germ Censorship | Tony Johnson
To those who say human sexual orientation is so complex, subject to so many variables that we can’t possibly ever hope to discover the etiology of male homosexuality, keep Cochran’s reminder of “birds do it, bees do it but Cole Porter didn’t” and the story of the wonderful singing red cicada:
http://hosted.ap.org/dynamic/stories/U/US_SCI_CICADA_INVASION?SITE=AP&SECTION=HOME&TEMPLATE=DEFAULT&CTIME=2013-05-06-14-19-13
If these bugs know precisely when to make their entrance after all those years underground and then know what to do to get a chance to mate, it really can’t be all that complicated.
Makes me wish I were on the East Coast when this happens. Must be quite the symphony (or cacophony), depending on one’s mood at the time.
Pingback: dakota
Pingback: Is homosexuality caused by a germ? | Julian O'Dea
Pingback: Greg Cochran’s “Gay Germ” Hypothesis – An Exercise in the Power of Germs | JayMan's Blog
I realize that most people here consider the neurological difference between homosexuals and heterosexuals to be a result of damage.
Pingback: The Origin of Homosexuality | Jason Bayz
Pingback: The Cause of Homosexuality | Jason Bayz
Pingback: Key Recent Papers and Postings | JayMan's Blog
Pingback: Greg Cochran’s “Gay Germ” Hypothesis – An Exercise in the Power of Germs – Saffron Storm Trooper